In canine hearts with inducible reentry, the isthmus tends to form along an axis from the area of last to first activity during sinus rhythm. It was hypothesized that this phenomenon could be quantified to predict reentry and the isthmus location. An in situ canine model of reentrant ventricular tachycardia occurring in the epicardial border zone was used in 54 experiments (25 canine hearts in which primarily long monomorphic runs of figure-8 reentry was inducible, 11 with short monomorphic or polymorphic runs, and 18 lacking inducible reentry). From the sinus rhythm activation map for each experiment, the linear regression coefficient and slope was calculated for the activation times along each of 8 rays extending from the area of last-activation. The slope of the regression line for the ray with greatest regression coefficient (called the primary axis) was used to predict whether or not reentry would be inducible (correct prediction in 48/54 experiments). For all 36 experiments with reentry, isthmus location and shape were then estimated based on site-to-site differences in sinus rhythm electrogram duration. For long and short-runs of reentry, estimated isthmus location and shape partially overlapped the actual isthmus (mean overlap of 71.3% and 43.6%, respectively). On average for all reentry experiments, a linear ablation lesion positioned across the estimated isthmus would have spanned 78.2% of the actual isthmus width. Parameters of sinus rhythm activation provide key information for prediction of reentry inducibility, and isthmus location and shape.
During ventricular tachycardia, the heart beats rapidly which can be debilitating to the patient and cause such things as tiredness and even syncope (i.e. fainting). This clinical problem usually follows a myocardial infarction (heart attack) and is caused by abnormal electrical conduction in the heart because the cells become damaged during the infarct. When conduction is slow and abnormal, a process called reentry can occur in which the propagating electrical wavefront travels in a circle, or double loop, and reenters the area where it had previously traveled. This propagation around the loop(s) occurs very rapidly, and a heartbeat occurs once each time the propagating wavefront traverses around the loop or loops. Since the condition is abnormal, the heart muscle does not contract as it should, so that the strength of the pumping action is reduced, and the rapidity of the heartbeat causes the heart chambers to not fill with blood completely. Therefore, because of both the poor filling action and the poor pumping action, there is less blood delivered to the tissues. This causes the maladies that the patient experiences.
A promising cure for this ailment is radio-frequency catheter ablation, which does not require surgery and is permanent. In the ablation procedure, a catheter is inserted through an artery of the patient and is positioned in the heart chamber. At the appropriate location on the inner heart surface, known as the endocardium, radio-frequency energy is delivered from the tip of the catheter to the heart tissue, thereby blocking conduction at the place of delivery of the energy, which is called the target site on the heart. Ideally, energy is delivered to the location between the double loop where the electrical wavefront propagates. This is called the best, or optimal target site. However, it is sometimes difficult to locate the best target site, and also the precise surface area to which energy should be delivered is often unknown and presently must be done by trial and error.
The present disclosure describes a system and method for determining the shape and location of the target site, which is called the reentry isthmus. U.S. Pat. No. 6,236,883 to Ciaccio et al describes a method to find the isthmus based on signals acquired while the heart was undergoing ventricular tachycardia.
Although this former method potentially represents a substantial improvement over existing methods, it is not always convenient and cannot be used in all cases. For example during clinical electrophysiologic (EP) study, in which the clinician endeavors to determine the target site to ablate the heart in the patient, it is attempted to initiate ventricular tachycardia by electrical stimulation. If tachycardia cannot be initiated, the former method described in the U.S. Pat. No. 6,236,883 to Ciaccio et al will not work because the methodology requires signals obtained from the heart surface during ventricular tachycardia. Furthermore, sometimes tachycardia can be initiated but there is poor hemodynamic tolerance, which means that the pumping of blood is so poor during the tachycardia that the doctor must terminate it so that the patient does not experience syncope. The method of the present disclosure addresses both problems.
In one embodiment of the present disclosure, the reentry isthmus may be localized and its shape may be estimated based on sinus-rhythm signals from the heart surface. Sinus-rhythm is the normal rhythm of the heart. Therefore, based on this methodology there may no longer be a need to induce ventricular tachycardia in the patient's heart during clinical EP study.
The method of the present disclosure provides the clinician with a target area to ablate the heart to stop reentrant ventricular tachycardia from recurring. Accuracy is important so that only those portions of the heart at which ablation is needed are actually ablated. Ablating other areas can increase the chance of patient morbidity, by damaging regions of the heart unnecessarily. Also, there is less chance that the patient will be required to have a repeat visit, which will reduce cost of the total procedure and reduce discomfort to the patient. Rapidity is important to reduce the amount of fluoroscopy time and therefore reduce the radiation exposure to the patient, as well as cost due to the reduction in time for the procedure, and patient discomfort.
The method of the present disclosure is also an advance over previous methods because there may be no need to acquire many signals directly from the heart surface which is difficult and time consuming, for the procedure. Instead, only the electrocardiogram (ECG) signal may be needed during tachycardia. This ECG signal may be obtained during the EP study, or even via a Holter Monitor when the patient is ambulatory and the heart undergoes an episode of tachycardia. Therefore, the method of the present disclosure may greatly improve the accuracy of targeting the best ablation site to stop reentrant ventricular tachycardia even when tachycardia cannot be induced or is hemodynamically stable, both of which occur in a significant number of patients.
Treatment of reentrant ventricular tachycardia by catheter ablation methods is hampered by the difficulty in localizing the circuit, particularly when the circuit structure is complex, the tachycardia is short-lived, or when reentry is not inducible during electrophysiologic study [1]. If measurements of sinus rhythm activation could be used to accurately localize reentry circuit features, it could potentially greatly improve the cure rate under these circumstances. A number of clinical and experimental studies to determine the usefulness of sinus rhythm parameters for targeting reentry circuits have been reported. The time of latest depolarization during sinus rhythm has been partially correlated to the location of the reentry isthmus; however, the relationship is inexact [2-3]. At the border zone, both normal and abnormal (low-amplitude, fractionated, or wide-deflection) electrograms are present [2-5]; however, these abnormal electrograms can be present both within and away from the reentry circuit location and are therefore not a specific predictor of its position in the border zone. Therefore, methods for detection and measurement of abnormal sinus rhythm activation characteristics are not presently sufficient for targeting reentry circuits for catheter ablation, although presence of abnormality suggests the proximity of arrhythmogenic substrate.
When a reentrant circuit can be induced in the infarct border zone by programmed electrical stimulation in a canine model [6], the area where the isthmus forms has at least two conspicuous substrate properties: 1) it is the thinnest surviving cell layer of any area of the border zone [6-7], and 2) there is disarray of gap-junctional intercellular connections which extends the full thickness from the infarct to the surface of the heart [8]. Since these substrate properties persist regardless of rhythm type, they may affect electrical conduction at the isthmus area during sinus rhythm. The hypothesis that these phenomena could be quantified and used to predict reentry inducibility, and isthmus location and shape, when it occurs, was tested in this study.